The peripheral neuropathies caused by acrylamide and vincristine ar being investigated using electrophysiological and histological techniques. Sensory and motor nerve susceptibility to the neurotoxicity of these agents is being determined and correlated withclinical sysmtmatology. The site of the initial neural lesion caused by these agents is also being investigated by studying the neuropathies resulting from their systemi versus localized administratio. This should provide an indication of involvement, if any, of anterior horn cells and dorsal root ganglia in the genesis of the neuropathy. These expermental neuropathies are being induced in cats. Present findings in acrylamide neuropathy indicate: 1) muscle spindle dysfunction precedes motor nerve deficit; 2)spindles have a decreased ability to signal higher centers o muscle length and the rate of change in muscle length; 3) onset of clinical signs of neuropayth coincide with changes in spindle function while motor nerve changes occur later; 4) degenerative changes in the dorsal root ganglia are observed. BIBLIOGRAPHIC REFERENCES: Lowndes, H.E. and Baker, T,: Motor nerve terminal function in acrylamide-induced peripheral neuropathy. Fed. Proc. 32: 75l: l975. Lowndes, H.E. and Baker, T.: DFP-induced sub-acute presynaptic alteration at the neuromusclar junction. Pharmacologist l7:245:l975.